Original Research

The fructose–copper connection: Added sugars induce fatty liver and insulin resistance via copper deficiency

James J. DiNicolantonio, Dennis Mangan, James H. O'Keefe
Journal of Insulin Resistance | Vol 3, No 1 | a43 | DOI: https://doi.org/10.4102/jir.v3i1.43 | © 2018 James J. DiNicolantonio | This work is licensed under CC Attribution 4.0
Submitted: 04 June 2018 | Published: 26 September 2018

About the author(s)

James J. DiNicolantonio, Department of Preventive Cardiology, Saint Luke’s Mid America Heart Institute, United States
Dennis Mangan, Independent Researcher, United States
James H. O'Keefe, Department of Preventive Cardiology, Saint Luke’s Mid America Heart Institute, United States


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Abstract

Background: Evidence suggests that the overconsumption of added sugars can induce fatty liver disease and insulin resistance.

Aim: To propose a hypothesis that added sugars induce copper deficiency which can lead to hepatic iron overload, fatty liver disease, insulin resistance and eventually non-alcoholic steatohepatitis.

Setting: On average, the intake of added sugars in humans is higher than levels that have been found to impair copper status in animals.

Methods: Narrative review.

Results: Fructose-induced copper deficiency may be a leading cause of fatty liver disease and insulin resistance.

Conclusion: The reduction in the intake of added sugars may improve copper status and reduce the risk of fatty liver disease and insulin resistance.


Keywords

copper; fructose; sucrose; sugar; fatty liver

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